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Vascular smooth muscle cell apoptosis induced by verapamiland the effect of cell apoptosis in the mechanism ofrestenosis after angioplasty

Chen Ji

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Abstract

AIM To investigate whether verapamil could induce vascular smooth muscle cell apoptosis and the effect of cell apoptosis in the mechanism of restenosis after angioplasty. METHODS Rabbit iliac artery atherosclerotic and restenotic models were made. The normal, atherosclerotic and restenotic iliac arteries were aseptically removed from rabbits for the cultures of iliac artery smooth muscle cell(SMC) respectively. Cell proliferation was examined with TdR incorporation and cell apoptosis was investigated in SMC treated with verapamil through the observation of cell morphology, DNA gel electrophoresis and flow cytometry. RESULTS The findings showed that the extent of proliferation activated increased by 26% and the extend of apoptosis activited increased by 19%; this might tip the balance between the two processes and the deletion of excessive SMC could not be made timely, thus, the restenosis will occur. CONCLUSIONTBZVerapamil can induce vascular smooth muscle apoptosis and SMC apoptosis may be involved in the pathogenesis of atherosclerotic and restenotic lessions; cell apoptosis activated to a lesser extent may play an improtant role in the mechanism of restenosis.

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AIM To investigate whether verapamil could induce vascular smooth muscle cell apoptosis and the effect of cell apoptosis in the mechanism of restenosis after angioplasty. METHODS Rabbit iliac artery atherosclerotic and restenotic models were made. The normal, atherosclerotic and restenotic iliac arteries were aseptically removed from rabbits for the cultures of iliac artery smooth muscle cell(SMC) respectively. Cell proliferation was examined with TdR incorporation and cell apoptosis was investigated in SMC treated with verapamil through the observation of cell morphology, DNA gel electrophoresis and flow cytometry. RESULTS The findings showed that the extent of proliferation activated increased by 26% and the extend of apoptosis activited increased by 19%; this might tip the balance between the two processes and the deletion of excessive SMC could not be made timely, thus, the restenosis will occur. CONCLUSIONTBZVerapamil can induce vascular smooth muscle apoptosis and SMC apoptosis may be involved in the pathogenesis of atherosclerotic and restenotic lessions; cell apoptosis activated to a lesser extent may play an improtant role in the mechanism of restenosis.

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Available abstract

AIM To investigate whether verapamil could induce vascular smooth muscle cell apoptosis and the effect of cell apoptosis in the mechanism of restenosis after angioplasty. METHODS Rabbit iliac artery atherosclerotic and restenotic models were made. The normal, atherosclerotic and restenotic iliac arteries were aseptically removed from rabbits for the cultures of iliac artery smooth muscle cell(SMC) respectively. Cell proliferation was examined with TdR incorporation and cell apoptosis was investigated in SMC treated with verapamil through the observation of cell morphology, DNA gel electrophoresis and flow cytometry. RESULTS The findings showed that the extent of proliferation activated increased by 26% and the extend of apoptosis activited increased by 19%; this might tip the balance between the two processes and the deletion of excessive SMC could not be made timely, thus, the restenosis will occur. CONCLUSIONTBZVerapamil can induce vascular smooth muscle apoptosis and SMC apoptosis may be involved in the pathogenesis of atherosclerotic and restenotic lessions; cell apoptosis activated to a lesser extent may play an improtant role in the mechanism of restenosis.

Key concepts: Restenosis, Apoptosis, Vascular smooth muscle, Cell, Flow cytometry, Pathogenesis, Verapamil, Cell biology

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